Tuesday, December 22, 2015

Casey Luskin is worried about university students. Apparently, they aren't getting enough correct information about intelligent design. Luskin uses the example of a student named Michael Heckle at Iowa State University. Mr. Heckel said; "So far, there has been no research done by intelligent design advocates that has led to any sort of scientific discovery."

You have to deny mountains of research and evidence to say that. Intelligent design advocates have done a great deal of research, leading to numerous scientific discoveries. Let's help out this student by reviewing some prominent ones, amounting to only a portion of that overall research.

This is going to be fun. Casey Luskin is about to reveal some ID research that has led to some sort of "scientific discovery."1

The first example that Casey Luskin quotes is Doug Axe's "discovery" that new protein folds cannot evolve. I'm not going to discuss that result. It's pretty obvious that if it were a new scientific discovery then half of my department would be idiots and Doug Axe would be in line for a Nobel Prize.

It's the second example I want to look at ....

In 2004, biochemist Michael Behe and physicist David Snoke published research in the journal Protein Science. They reported the results of computer simulations of the evolution of protein-protein interactions. Vital to virtually all cellular processes, these interactions require a specific "hand in glove" fit, where multiple amino acids must be properly ordered to allow the three-dimensional connection. The simulations showed that the Darwinian evolution of a simple bond between two proteins would be highly unlikely to arise in populations of multicellular organisms if it required two or more mutations to function. They concluded that "the mechanism of gene duplication and point mutation alone would be ineffective...because few multicellular species reach the required population sizes."

Let's look at the paper by Behe and Snoke (2004). (David Snoke is a professor of physics at the University of Pittsburgh.) It's not exactly what Casey Luskin describes. In fact it has nothing to do with protein-protein interactions.

Behe & Snoke looked at the evolution of a new protein function following a gene duplication event. They wanted to model two competing processes. In one situation the "death" of one of the duplicates occurs when it acquires a deleterious mutation. (Shown as a red "x" in the figure.) The probability of such an event is the product of the mutation rate (v ) and the fraction of the mutations that will be deleterious over the entire sequence of the gene (p).

In the other situation, a new gene with a new function is born. In the simplest model they imagine that this "birth" requires three specific mutations in various parts of the gene. The probability is determined by the product of the mutation rate and the number of sites that need to be changed (λ). The example in the figure shows a situation where three amino acid residues have to be changed (green) (λ=3). (The loci could be anywhere in the sequence ... they don't have to be adjacent as shown in the figure.)

The goal is to find out whether the evolution of a "mutliresidue" (MR) feature is possible given standard mutation rates and population sizes. Here's how Behe & Snoke introduce the paper:

Although many scientists assume that Darwinian processes account for the evolution of complex biochemical systems, we are skeptical. Thus, rather than simply assuming the general efficacy of random mutation and selection, we want to examine, to the extent possible, which changes are reasonable to expect from a Darwinian process and which are not. We think the most tractable place to begin is with questions of protein structure. Our approach is to examine pathways that are currently considered to be likely routes of evolutionary development and see what types of changes Darwinian processes may be expected to promote along a particular pathway.

The analysis begins by assuming that the population consists of individuals with a recently duplicated gene. They assume haploid organisms reproducing asexually with no recombination.

The model is going to examine the competition between mutations that "kill" the gene and a combination of mutations that create a gene with a new function. Each of the mutations that will collectively give rise to a new function will disrupt the original function ... it's only when all of the mutations are present that a new gene is born. We will see that this is the assumption that causes the most problems for the model.

The pertinent feature of the model is that multiple changes are required in the gene before the new, selectable feature appears. Changes in these nucleotide positions are assumed to be individually disruptive of the original function of the protein but are assumed either to enhance the original function or to confer a new function once all are in the compatible state. Thus, the mutations would be strongly selected against in an unduplicated gene, because its function would be disrupted and no duplicate would be available to back up the function.

Keep in mind that their model only looks at situations where just one combination of substitutions will work. The parameter, λ, can be 2, 3, 4, or more. It is the total number of different sites that must be changed. These are the "compatible" sites.

The mutation rates of all mutations are the same. One of the important parameters is p—the ratio of deleterious mutations and compatible mutations. If there are 2400 possible deleterious mutations and three compatible sites then p = 2400/3 = 800. (Neutral mutations are ignored.)

The model estimates the average time (Tf) to the first occurrence of the genes with the new function. Tf is the number of generations until the last of the required mutations occur.

The new combination of mutations (= multiresidue feature (MR)) will give rise to a new function with a selection coefficient of s. The new allele will become fixed with a probability of about 2s so the complete equation is:

Behe & Snoke assume that the mutation rate is 10-8 (v=10-8). The actual per nucleotide mutation rate is 10-10 per replication so their value will be off by two orders of magnitude in single-cell organisms but closer to the actual per generation value for large multicellular organisms.

They assume that the ratio of deleterious substitutions to compatible substitutions is 1000 (p=1000). (We'll see in my next post that this value is too high by several orders of magnitude.)

They assume s=0.01. This is a reasonable assumption.

Behe & Snoke calculate the average time to fixation (in generations) for several values of λ and several different population sizes (N). The results are shown in Figure 6 of their paper.

I've added red lines to indicate how we should interpret this figure. For the situation where three different mutations are required (λ=3) for the new function, we can estimate the population size necessary for fixation after 100 million generations (Tfx=108). That value is about 1011 (N~1011).

If the generation time is one year then this means that in order to fix the new gene in 100 million years it would require a population size of 100 billion organisms. This is very unlikely. Behe & Snoke's main point is that the evolution of any new function requires multiple mutations and the probability of these MR features arising in a reasonable time is far too low to be effective—unless you postulate huge population sizes that are far greater than anything we know for most species.

This is an anti-evolution argument. They do not suggest a solution.

The authors admit that some of their estimates might be wrong. They have assumed a population that has already fixed a duplicated gene locus with both copies functional. They claim that their final values of Tfx are underestimates because they should be taking into account the time it takes for the duplicated genes to reach appreciable frequency in the population.

On the other hand, they have assumed that there is only one pathway to a new gene function but there might actually be several different pathways involving a number of different amino acid residues. For example, the new function might require a disulfide bond. Behe & Stoke assume that there are only two possible residues that could mutate to cysteine in order to form such a bond (λ=2 in this case). However, there may be several different residues that could mutate to cysteine so their calculations may exaggerate the difficulty in forming a new function.

They recognize that their value of p (p=1000) might be too high but they claim that it is "conservative" relative to the values used by others. They recognize that the model is sensitive to the value of λ but they quote several examples where new functions require three or more different mutations. Furthermore, even if only two mutations were required it still takes a population size of 10 million to fix the mutations in 100 million years and this is beyond the edge of evolution for most populations.

If Behe & Snoke are correct then this is an amazing result. It means that modern evolutionary theory cannot explain the origins of any new function that requires three or more independent mutations.

But Behe & Snoke are not correct (surprise!). The paper was thoroughly refuted and discredited by Michael Lynch in an article published in the same journal one year later [see the Wikipedia article at: Behe and Snoke, 2004].

In my next post I'll discuss the Lynch paper and Behe's response.

1. The most important scientific discovery we learn from ID research is that ID proponents are stupid and/or incompetent. I don't think that's what Casey Luskin means.

1. Jensen admits that his expertise in population genetics is limited, from his review cited by Torley:

Reading this book made me realize that I do not have a strong enough foundation in population genetics to really assess the validity of Provine’s argument. I am sorry for leading you along so far, just to say I don’t know. But I don’t, and that’s because I am not familiar enough with the population genetics literature to determine whether Provine’s depiction of the field is accurate.

2. As a matter of fact, Prof. Moran has commented on Provine's claims back in August of this year. His take and that of most of his commentors appears to be that Provine's arguments are hard to understand and are stated in obscure language. Not being a biologist, I have no opinion on the subject.

I note, however, that the book is self published. It would be interesting if he has published or attempt to publish papers in the peer reviewed literature where his ideas could be vetted by expert reviewers.

"At the same time Casey Luskin tries to boast about all the scientific work published by ID advocates, the flagship scientific journal for the movement has only published a single paper in calendar year 2015, despite getting a new editor and having an editorial board with 29 members."

The "flagship scientific journal for the movement" is only allowed to be used by those who are associated with an academic institution that the Discovery Institute wants to flaunt. Therefore I am forbidden to publish my "theory of intelligent design" in the "science journal" for the "theory of intelligent design".

Interested in submitting to BIO-Complexity? We recommend that you review the About page for the journal's section policies, as well as the Author Guidelines. Authors need to register with BIO-Complexity prior to submitting. To be registered, send an email from an institutional or corporate account to our support address, or if already registered simply log in and begin the 5 step process.

The "flagship scientific journal for the movement" is only allowed to be used by those who are associated with an academic institution that the Discovery Institute wants to flaunt. Therefore I am forbidden to publish my "theory of intelligent design" in the "science journal" for the "theory of intelligent design".

Interested in submitting to BIO-Complexity? We recommend that you review the About page for the journal's section policies, as well as the Author Guidelines. Authors need to register with BIO-Complexity prior to submitting. To be registered, send an email from an institutional or corporate account to our support address, or if already registered simply log in and begin the 5 step process.

I was about to write that BioComplexity has not published an issue in the past year, but then I checked their website and - will wonders never cease? - they actually have a new issue out! It's simply referred to as "Vol. 2015" and consists of one whole article by one Winston Ewart, whose institutional affiliation is listed as, well let's check.... What do you know, "The Biologic Institute"! What are the odds?

With all the "mountains" of ID research being done, you know BioComplexity is giving you only the crème de la crème if it only publishes a single article in an entire year.

There are no "mountains of research and evidence" in what Casey linked to. It's absolutely depressing to see him making a fool out of me, while still making a fool out of himself by repeating the same old garbage that already caused so much trouble in Dover:

You have to deny mountains of research and evidence to say that. Intelligent design advocates have done a great deal of research, leading to numerous scientific discoveries. Let's help out this student by reviewing some prominent ones, amounting to only a portion of that overall research. (For a complete listing of pro-ID peer-reviewed publications, see: Peer-Reviewed Articles Supporting Intelligent Design.)

Laurence A. Moran

Larry Moran is a Professor Emeritus in the Department of Biochemistry at the University of Toronto. You can contact him by looking up his email address on the University of Toronto website.

Sandwalk

The Sandwalk is the path behind the home of Charles Darwin where he used to walk every day, thinking about science. You can see the path in the woods in the upper left-hand corner of this image.

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Some readers of this blog may be under the impression that my personal opinions represent the official position of Canada, the Province of Ontario, the City of Toronto, the University of Toronto, the Faculty of Medicine, or the Department of Biochemistry. All of these institutions, plus every single one of my colleagues, students, friends, and relatives, want you to know that I do not speak for them. You should also know that they don't speak for me.

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Quotations

The old argument of design in nature, as given by Paley, which formerly seemed to me to be so conclusive, fails, now that the law of natural selection has been discovered. We can no longer argue that, for instance, the beautiful hinge of a bivalve shell must have been made by an intelligent being, like the hinge of a door by man. There seems to be no more design in the variability of organic beings and in the action of natural selection, than in the course which the wind blows.Charles Darwin (c1880)Although I am fully convinced of the truth of the views given in this volume, I by no means expect to convince experienced naturalists whose minds are stocked with a multitude of facts all viewed, during a long course of years, from a point of view directly opposite to mine. It is so easy to hide our ignorance under such expressions as "plan of creation," "unity of design," etc., and to think that we give an explanation when we only restate a fact. Any one whose disposition leads him to attach more weight to unexplained difficulties than to the explanation of a certain number of facts will certainly reject the theory.

Charles Darwin (1859)Science reveals where religion conceals. Where religion purports to explain, it actually resorts to tautology. To assert that "God did it" is no more than an admission of ignorance dressed deceitfully as an explanation...

Quotations

The world is not inhabited exclusively by fools, and when a subject arouses intense interest, as this one has, something other than semantics is usually at stake.
Stephen Jay Gould (1982)
I have championed contingency, and will continue to do so, because its large realm and legitimate claims have been so poorly attended by evolutionary scientists who cannot discern the beat of this different drummer while their brains and ears remain tuned to only the sounds of general theory.
Stephen Jay Gould (2002) p.1339
The essence of Darwinism lies in its claim that natural selection creates the fit. Variation is ubiquitous and random in direction. It supplies raw material only. Natural selection directs the course of evolutionary change.
Stephen Jay Gould (1977)
Rudyard Kipling asked how the leopard got its spots, the rhino its wrinkled skin. He called his answers "just-so stories." When evolutionists try to explain form and behavior, they also tell just-so stories—and the agent is natural selection. Virtuosity in invention replaces testability as the criterion for acceptance.
Stephen Jay Gould (1980)
Since 'change of gene frequencies in populations' is the 'official' definition of evolution, randomness has transgressed Darwin's border and asserted itself as an agent of evolutionary change.
Stephen Jay Gould (1983) p.335
The first commandment for all versions of NOMA might be summarized by stating: "Thou shalt not mix the magisteria by claiming that God directly ordains important events in the history of nature by special interference knowable only through revelation and not accessible to science." In common parlance, we refer to such special interference as "miracle"—operationally defined as a unique and temporary suspension of natural law to reorder the facts of nature by divine fiat.
Stephen Jay Gould (1999) p.84

Quotations

My own view is that conclusions about the evolution of human behavior should be based on research at least as rigorous as that used in studying nonhuman animals. And if you read the animal behavior journals, you'll see that this requirement sets the bar pretty high, so that many assertions about evolutionary psychology sink without a trace.

Jerry Coyne
Why Evolution Is TrueI once made the remark that two things disappeared in 1990: one was communism, the other was biochemistry and that only one of them should be allowed to come back.

Sydney Brenner
TIBS Dec. 2000
It is naïve to think that if a species' environment changes the species must adapt or else become extinct.... Just as a changed environment need not set in motion selection for new adaptations, new adaptations may evolve in an unchanging environment if new mutations arise that are superior to any pre-existing variations

Douglas Futuyma
One of the most frightening things in the Western world, and in this country in particular, is the number of people who believe in things that are scientifically false. If someone tells me that the earth is less than 10,000 years old, in my opinion he should see a psychiatrist.

Francis Crick
There will be no difficulty in computers being adapted to biology. There will be luddites. But they will be buried.

Sydney Brenner
An atheist before Darwin could have said, following Hume: 'I have no explanation for complex biological design. All I know is that God isn't a good explanation, so we must wait and hope that somebody comes up with a better one.' I can't help feeling that such a position, though logically sound, would have left one feeling pretty unsatisfied, and that although atheism might have been logically tenable before Darwin, Darwin made it possible to be an intellectually fulfilled atheist

Richard Dawkins
Another curious aspect of the theory of evolution is that everybody thinks he understand it. I mean philosophers, social scientists, and so on. While in fact very few people understand it, actually as it stands, even as it stood when Darwin expressed it, and even less as we now may be able to understand it in biology.

Jacques Monod
The false view of evolution as a process of global optimizing has been applied literally by engineers who, taken in by a mistaken metaphor, have attempted to find globally optimal solutions to design problems by writing programs that model evolution by natural selection.